AI Article Synopsis
- TIG1 is a gene linked to cell differentiation and cancer formation, which shows abnormal methylation patterns in various cancers.
- The research reveals that TIG1 interacts with another protein, cathepsin V (CTSV), leading to decreased stability of CTSV and affecting the activity of uPA, which is important for cell migration and invasion.
- Ectopic expression studies indicate that while CTSV enhances uPA activity and cellular movement, TIG1 can counteract these effects, suggesting a regulatory role for TIG1 in the uPA signaling pathway mediated by CTSV.
Article Abstract
Tazarotene-induced gene 1 (TIG1) is a retinoid acid receptor-responsive gene involved in cell differentiation and tumorigenesis. Aberrant methylation of CpG islands in the TIG1 promoter is found in multiple cancers. Currently, the exact mechanism underlying the anticancer effect of TIG1 is unknown. Here, we show that TIG1 interacts with cathepsin V (CTSV), which reduces CTSV stability and subsequently affects the production of activated urokinase-type plasminogen activator (uPA), an epithelial-mesenchymal transition-associated protein. Ectopic expression of CTSV increased the expression of activated uPA and the number of migrated and invaded cells, whereas ectopic TIG1 expression reversed the effects of CTSV on the uPA signaling pathway. Similar patterns in the production of activated uPA and number of migrated and invaded cells were also observed in TIG1-expressing and CTSV-knockdown cells. The results suggest that CTSV may participate in TIG1-regulated uPA activity and the associated downstream signaling pathway.
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| http://dx.doi.org/10.1007/s12013-020-00940-3 | DOI Listing |
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